Sudden cardiac arrest (SCA) outside the hospital is a leading cause of death in the western world, and globally the incidence is estimated to 55 per 100 000 person-years. The number of patients surviving to hospital discharge remains low. A recent meta-analysis stated the aggregate survival rate to hospital discharge to be 7.6%, which has not significantly changed in almost 30 years.
Chest compression during cardiopulmonary resuscitation (CPR) remains one of few proven treatments for patients suffering from sudden cardiac arrest, supplying blood to the critical organs—brain and heart-muscle—until spontaneous circulation hopefully resumes. It has been shown that a higher quality of CPR improves the outcome. In both experimental and clinical studies chest compressions before defibrillation attempts increase the chance both of successful defibrillation and survival. The compression profile (how rapidly the chest is compressed and decompressed), frequency, depth and duty cycle of the chest compressions affect the blood flow and pressures obtained during CPR.
The quality of CPR can now be measured by accelerometers and transthoracic impedance, and the quality of manual CPR given by professionals has been found to be substantially below international recommendations. Mechanical chest compression devices have the potential to improve these factors. They can give consistent chest compressions, can free the personnel to accomplish other chores and can be used during transport where high quality manual compressions are impossible and are dangerous for the medical personnel who in that case cannot be belted in the vehicle. Chest compression devices can also enable chest compressions during interventions on the coronary arteries in the catheter laboratory. The ideal function and properties of such devices are far from determined at present.
There are two theories for the mechanism of blood flow generation from chest compressions; (i) the cardiac pump theory—which suggests that the heart is squeezed between the breast-bone and the backbones—and (ii) the thoracic pump theory—where the whole chest functions as a pump due to pressure changes within the chest generated by the chest compressions. The clinical effect is most likely varied combinations of the two.
U.S. Pat. No. 6,398,745 and US 2012/191025 are examples of a known type of chest compression device where a belt around the patient's chest is tightened and relaxed by a belt-tightening spool and electric motor. Published randomized clinical outcome studies so far have not shown a clear improvement in patient survival with a device based on this principle.
US 2003/181834 describes a chest compression device with a plate positioned behind the patient's back and a two-legged front part that can be attached to the back plate. The front part includes a chest compressor which exerts pressure on the breastbone. The arrangement shown in this publication is similar to commercially available chest compression devices, such as the LUCAS™ Chest Compression System manufactured and developed by Jolife AB/Physio-Control of Sweden. U.S. Pat. No. 8,002,720 discloses another similar device.